PMID- 16290189 OWN - NLM STAT- MEDLINE DCOM- 20060503 LR - 20181113 IS - 1063-4584 (Print) IS - 1522-9653 (Electronic) IS - 1063-4584 (Linking) VI - 14 IP - 3 DP - 2006 Mar TI - Regulation of matrix metalloproteinase expression by dynamic tensile strain in rat fibrochondrocytes. PG - 264-72 AB - OBJECTIVE: We sought to determine the molecular basis for the anticatabolic effects of mechanical signals on fibrocartilage cells by studying the expression of a variety of matrix metalloproteinases (MMPs). Furthermore, we examined whether the effects of biomechanical strain on MMP gene expression are sustained. METHODS: Fibrochondrocytes from temporomandibular joint (TMJ) discs were exposed to dynamic tensile strain for various time intervals in the presence of interleukin (IL)-1beta. The regulation of the messenger RNA (mRNA) expression and synthesis of MMPs and tissue inhibitors of MMPs (TIMPs) were examined by end-point and real-time reverse transcriptase-polymerase chain reaction (RT-PCR) as well as Western blot analysis. RESULTS: Fibrochondrocytes expressed mRNA for MMP-2, -3, -7, -8, -9, -11, -13, -14, -16, -17, and -19 as well as TIMP-1, -2, and -3, IL-1beta induced a significant (P<0.05) upregulation of mRNA for MMP-3, -7, -8, -9, -13, -16, -17, and -19. The IL-1beta-stimulated upregulation of these MMPs was significantly (P<0.05) abrogated by dynamic tensile strain. However, MMP-2, -11, -14, and TIMPs were not affected by either IL-1beta or tensile strain. Biomechanical strain also inhibited the IL-1beta-stimulated protein synthesis of MMP-3, -7, -8, -9, -13, -16, and -17. Application of mechanical strain for various time intervals during a 24-h incubation with IL-1beta showed that the suppressive effects of mechanical signals are sustained. CONCLUSIONS: The data provide evidence that biomechanical signals can downregulate the catabolic activity of fibrocartilage cells in an inflammatory environment by inhibiting the expression of a variety of MMPs. Furthermore, the matrix-protective effects of biomechanical signals are sustained even in an inflammatory environment. FAU - Deschner, J AU - Deschner J AD - The Ohio State University, Oral Biology and Orthopedics, 4171 Postle Hall, 305 West 12th Avenue, Columbus, OH 43210, USA. FAU - Rath-Deschner, B AU - Rath-Deschner B FAU - Agarwal, S AU - Agarwal S LA - eng GR - R01 DE015399/DE/NIDCR NIH HHS/United States GR - DE15399/DE/NIDCR NIH HHS/United States GR - R01 AT000646/AT/NCCIH NIH HHS/United States GR - DE13799/DE/NIDCR NIH HHS/United States GR - AT000646/AT/NCCIH NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20051114 PL - England TA - Osteoarthritis Cartilage JT - Osteoarthritis and cartilage JID - 9305697 RN - 0 (Interleukin-1) RN - 0 (RNA, Messenger) RN - 0 (Tissue Inhibitor of Metalloproteinases) RN - EC 3.4.24.- (Matrix Metalloproteinases) SB - IM MH - Animals MH - Blotting, Western MH - Cells, Cultured MH - Chondrocytes/*enzymology/metabolism MH - Down-Regulation/physiology MH - Fibrocartilage/cytology/*enzymology/metabolism MH - Gene Expression Regulation, Enzymologic/*physiology MH - Interleukin-1/pharmacology MH - Matrix Metalloproteinases/*biosynthesis/genetics MH - Mechanotransduction, Cellular/*physiology MH - RNA, Messenger/genetics MH - Rats MH - Rats, Sprague-Dawley MH - Reverse Transcriptase Polymerase Chain Reaction/methods MH - Stress, Mechanical MH - Temporomandibular Joint/cytology/enzymology/metabolism MH - Tissue Inhibitor of Metalloproteinases/biosynthesis/genetics PMC - PMC4948984 MID - NIHMS801995 EDAT- 2005/11/18 09:00 MHDA- 2006/05/04 09:00 PMCR- 2016/07/18 CRDT- 2005/11/18 09:00 PHST- 2005/02/04 00:00 [received] PHST- 2005/09/14 00:00 [accepted] PHST- 2005/11/18 09:00 [pubmed] PHST- 2006/05/04 09:00 [medline] PHST- 2005/11/18 09:00 [entrez] PHST- 2016/07/18 00:00 [pmc-release] AID - S1063-4584(05)00261-X [pii] AID - 10.1016/j.joca.2005.09.005 [doi] PST - ppublish SO - Osteoarthritis Cartilage. 2006 Mar;14(3):264-72. doi: 10.1016/j.joca.2005.09.005. Epub 2005 Nov 14.